Repetitive Head Impacts: A Concern At All Levels of Sports


Lindsey Barton Straus

More troubling findings 

Most recently, a remarkable series of eight studies [31-38] by Purdue scientists as part of an ongoing study of brain changes in high school football players, made a host of significant findings:

In the end, what the Purdue scientists found was that "concussed and non-concussed athletes look awfully similar, but that both look quite different from those who are not exposed to repetitive head collisions," said Talavage.

Perhaps most concerning, four of the Purdue studies found that damage to the brain from RHI persisted after the football season was over, as did a 2014 study by Bazarian and his URMC colleagues,[23], which found changes in brain white matter in a small group of college football players which persisted six months after the season was over. They found a strong correlation between the white matter changes and the number of head hits with a peak rotational acceleration exceeding 4500 rad/sec2 and the number of head hits with a peak rotational acceleration exceeding 6,000 rad/sec2, and an especially strong correlation where the number of the former exceeded 30-40 for the season, and the number of the latter exceeded 10-15 for the season. (For reference, a person nodding his head up and down as fast as possible produces a rotational acceleration of approximately 180 rads/sec2).

That six months off may not be long enough for the brains of football players to completely heal after a single season, putting them at even greater risk of head injury the next season, was concerning, said Bazarian.

"I don't want to be an alarmist, but this is something to be concerned about.  At this point we don't know the implications, but there is a valid concern that six months of no-contact rest may not be enough for some players," he said. "And the reality of high school, college and professional athletics is that most players don't actually rest during the off-season. They continue to train and push themselves and prepare for the next season."    

The findings of the first Purdue study alone were troubling, said Larry J. Leverenz, PhD, ATC, a Clinical Professor in the school's Department of Health and Kinesiology, shortly after the study was published, because it meant that players were:

Commenting at the time on the 2010 Purdue study for Sports Illustrated [15], Randall Benson, a neurologist at Wayne State University in Detroit, speculated that the Purdue researchers may have taken what amounted to a "real-time snapshot" of the early stages of the corrosive creep that wears away at the frontal lobe, a part of the brain involved in navigating social situations. Too much erosion and victims reach a breaking point - like former Steelers offensive lineman Terry Long, who died in 2005 from drinking antifreeze. "It's an insidious progression," Benson said, "and it's not obvious when you talk to [players]."

Four years later, Benson's speculation was echoed in eerily similar comments by Bazarian and his colleagues in the 2014 URMC study: "[i]f RHIs are related to neurodegeneration many years later, a long clinically silent period between the onset of neuronal injury and overt symptoms of dementia would not be unexpected." During this clinically silent period, however, there may be indicators of dysfunction on a cellular level, such as the elevated levels of S100B antibody found in the cerebral spinal fluid in the football players in the study, even six months after the end of the season, which he said, could "potentially herald[ ] the early stages of [chronic traumatic encephalopathy] or CTE."

"Pending confirmation in a long term longitudinal study tracking athletes prospectively for years to decades looking for manifestations of early cognitive dysfunction and dementia," writes Bazarian, "we believe our results suggest that these persistent DTI changes are likely detrimental.  If borne out in future research, the long-term persistence of these [white matter] changes would mean that athletes returning to play the following season would be at risk for expanded RHI-related WM changes, undetectable by conventional assessments. Could the lack of WM recovery we observed result in cumulative WM damage with subsequent football seasons of RHI exposures? If so, could this cumulative WM damage be related to the long-term development of CTE?"

Commenting on the recent series of Purdue studies for Purdue News,[30] Eric Nauman, a professor of mechanical engineering, basic medical sciences and biomedical engineering, and author or co-author of all 10 of the Purdue studies, said he was "particularly disturbed that when you get to the offseason, - we are looking somewhere between two and four months after the season has ended - the majority of players are still showing that they had not fully recovered."